Tregs and persistent

Poor oral health is commonly linked to cardiovascular disease through the established association between periodontitis and systemic inflammation. This relationship is usually explained by bacterial dissemination from periodontal pockets, lipid dysregulation, and oxidative stress, all of which may contribute to endothelial dysfunction and atherothrombotic changes. However, this conventional framework leaves an important question unresolved: if the main infectious and inflammatory niches are removed after complete tooth loss (edentulism), how does edentulism remain associated with increased cardiovascular risk? Epidemiological studies consistently show that edentulous individuals continue to have elevated cardiovascular morbidity and mortality, yet mechanistic explanations for this association remain underdeveloped. Therefore, this paper proposes a plausible biological model to explain persistent cardiovascular risk in edentulism. The model argues that, after tooth loss, the oral environment is not biologically inert but rather reorganised into a distinct ecological and immunological niche shaped by dentures, altered salivary flow, nutrient changes, microtrauma, and residual soft-tissue biofilms. The tongue, oral mucosa, saliva, and denture surfaces may support persistent colonisation by